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Identification
Name Fluvastatin
Accession Number DB01095 (APRD00346)
Type small molecule
Groups approved
Description

Fluvastatin is an antilipemic agent that competitively inhibits hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. HMG-CoA reducuase catalyzes the conversion of HMG-CoA to mevalonic acid, the rate-limiting step in cholesterol biosynthesis. Fluvastatin belongs to a class of medications called statins and is used to reduce plasma cholesterol levels and prevent cardiovascular disease.
Structure Thumb
Download: MOL | SDF | SMILES | InChI
Display: 2D Structure | 3D Structure
Synonyms
Fluindostatin
Fluvastatin sodium
Fluvastatina [INN-Spanish]
Fluvastatine [INN-French]
Fluvastatinum [INN-Latin]
Salts Not Available
Brand names
Name Company
Canef AstraZeneca
Cranoc Astellas
Lescol Novartis Pharmaceuticals
Lescol XL Novartis Pharmaceuticals
Brand mixtures Not Available
Categories
  • Anticholesteremic Agents
  • HMG-CoA Reductase Inhibitors
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
CAS number 93957-54-1
Weight Average: 411.4659
Monoisotopic: 411.18458653
Chemical Formula C24H26FNO4
InChI Key InChIKey=FJLGEFLZQAZZCD-JUFISIKESA-N
InChI
InChI=1S/C24H26FNO4/c1-15(2)26-21-6-4-3-5-20(21)24(16-7-9-17(25)10-8-16)22(26)12-11-18(27)13-19(28)14-23(29)30/h3-12,15,18-19,27-28H,13-14H2,1-2H3,(H,29,30)/b12-11+/t18-,19-/m0/s1
Plain Text
IUPAC Name
(3S,5R,6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid
SMILES
CC(C)N1C(\C=C\[C@H](O)C[C@H](O)CC(O)=O)=C(C2=CC=C(F)C=C2)C2=CC=CC=C12
Plain Text
Mass Spec Not Available
Taxonomy
Kingdom Organic
Classes
  • Statins
Substructures
  • Statins
  • Hydroxy Compounds
  • Alkanes and Alkenes
  • Acetates
  • Indoles and Indole Derivatives
  • Phenylpropenes
  • Pyrroles
  • Benzene and Derivatives
  • Carboxylic Acids and Derivatives
  • Halobenzenes
  • Heterocyclic compounds
  • Aromatic compounds
  • Imines
  • Alcohols and Polyols
  • Aryl Halides
Pharmacology
Indication To be used as an adjunct to dietary therapy to prevent cardiovascular events. May be used as secondary prevention in patients with coronary heart disease (CHD) to reduce the risk of requiring coronary revascularization procedures, for reducing progression of coronary atherosclerosis in hypercholesterolemic patients with CHD, and for the treatment of primary hypercholesterolemia and mixed dyslidipidemia.
Pharmacodynamics Fluvastatin, the first synthetically-derived HMG-CoA reductase inhibitor, is a hydrophilic, acidic, antilipemic agent used to lower cholesterol and triglyceride levels associated with primary hypercholesterolemia and mixed dyslipidemia (Fredrickson types IIa and IIb), to slow the progression of coronary atherosclerosis in patients with CHD and as secondary prevention therapy in patients with CHD to reduce the risk of requiring coronary revascularization procedures. Although similar to lovastatin, simvastatin, and pravastatin, fluvastatin has a shorter half-life, no active metabolites, extensive protein binding, and minimal CSF penetration. Fluvastatin acts primarily in the liver. It is prepared as a racemate of two erythro enantiomers of which the 3R,5S enantiomer exerts the pharmacologic effect.
Mechanism of action Fluvastatin selectively and competitively inhibits the hepatic enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. HMG-CoA reductase is responsible for converting HMG-CoA to mevalonate, the rate-limiting step in cholesterol biosynthesis. Inhibition results in a decrease in hepatic cholesterol levels which stimulates the synthesis of LDL receptors and increases hepatic uptake of LDL cholesterol. The end result is decreased levels of plasma total and LDL cholesterol.
Absorption Rapidly and almost completely absorbed (> 90%), but undergoes extensive first pass metabolism. Bioavailability is 24% (range 9-50%).
Volume of distribution
  • 0.35 L/kg
Protein binding 98% bound to plasma proteins
Metabolism
Undergoes hepatic metabolism primarily via hydroxylation of the indole ring at the 5- and 6-positions to 5-hydroxy fluvastatin and 6-hydroxy fluvastatin, respectively. N-dealkylation to N-desisopropyl fluvastatin and beta-oxidation of the side chain also occurs. Metabolized primarily by the CYP2C9 isozyme system (75%), and to a lesser extent by CYP3A4 (~20%) and CYP2C8 (~5%). Hydroxylated metabolites retain some pharmcological activity, but are present as conjugates (glucuronides and sulfates) in the blood and are rapidly eliminated via bile into feces.

Important The metabolism module of DrugBank is currently in beta. Questions or suggestions? Please contact us.

Substrate Enzymes Product
Fluvastatin
6-Hydroxyfluvastatin Details
Fluvastatin
N-Deisopropyl-fluvastatin Details
Fluvastatin
5-Hydroxyfluvastatin Details
Route of elimination Fluvastatin is metabolized in the liver, primarily via hydroxylation of the indole ring at the 5- and 6-positions. In vitro studies demonstrated that fluvastatin undergoes oxidative metabolism, predominantly via 2C9 isozyme systems (75%). No significant (<6%) renal excretion of fluvastatin occurs in humans.
Half life 1-3 hours
Clearance
  • 0.8 L/h/kg
  • 107 +/- 38.1 L/h [Hypercholesterolemia patients receiving a single dose of 20 mg]
  • 87.8 +/- 45 L/h [Hypercholesterolemia patients receiving 20 mg twice daily]
  • 108 +/- 44.7 L/h [Hypercholesterolemia patients receiving 40 mg single]
  • 64.2 +/- 21.1 L/h [Hypercholesterolemia patients receiving 40 mg twice daily]
Toxicity Generally well-tolerated. May cause GI upset (diarrhea, nausea, constipation, gas, abdominal pain), myotoxicity (mypothy, myositis, rhabdomyolysis), and hepatotoxicity.
Affected organisms
  • Humans and other mammals
Pathways
Pathway Name SMPDB ID
Smp00119 Fluvastatin Pathway SMP00119
Pharmacoeconomics
Manufacturers
  • Novartis pharmaceuticals corp
Packagers
Dosage forms
Form Route Strength
Capsule Oral 20 mg
Capsule Oral 40 mg
Tablet, extended release Oral 80 mg
Prices
Unit description Cost Unit
Lescol XL 80 mg 24 Hour tablet 4.25 USD tablet
Lescol xl 80 mg tablet 4.24 USD tablet
Lescol xl 80 mg tablet sa 3.66 USD tablet
Lescol 20 mg capsule 3.38 USD capsule
Lescol 40 mg capsule 3.37 USD capsule
Lescol Xl 80 mg Extended-Release Tablet 1.62 USD tablet
Lescol 40 mg Capsule 1.35 USD capsule
Lescol 20 mg Capsule 0.96 USD capsule
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
Patents
Country Patent Number Approved Expires (estimated)
United States 6242003 2000-10-13 2020-10-13
United States 5354772 1994-10-11 2011-10-11
Canada 2346868 2008-09-09 2019-10-12
Canada 2085037 2000-11-28 2012-12-10
Properties
State solid
Experimental Properties
Property Value Source
melting point 194-197 °C Not Available
water solubility 0.46 mg/L Not Available
logP 4.5 Not Available
Predicted Properties
Property Value Source
water solubility 4.41e-03 g/l ALOGPS
logP 3.69 ALOGPS
logP 3.83 ChemAxon
logS -5 ALOGPS
pKa (strongest acidic) 4.56 ChemAxon
pKa (strongest basic) -2.8 ChemAxon
physiological charge -1 ChemAxon
hydrogen acceptor count 4 ChemAxon
hydrogen donor count 3 ChemAxon
polar surface area 82.69 ChemAxon
rotatable bond count 8 ChemAxon
refractivity 114.86 ChemAxon
polarizability 44.31 ChemAxon
References
Synthesis Reference Not Available
General Reference Not Available
External Links
Resource Link
KEGG Compound C07014 Link_out
PubChem Compound 1548972 Link_out
PubChem Substance 46505668 Link_out
ChemSpider 1265982 Link_out
ChEBI 5136 Link_out
ChEMBL 5136 Link_out
Therapeutic Targets Database DAP000554 Link_out
PharmGKB PA449688 Link_out
Drug Product Database 2250527 Link_out
RxList http://www.rxlist.com/cgi/generic2/fluvastatinxl.htm Link_out
Drugs.com http://www.drugs.com/cdi/fluvastatin.html Link_out
Wikipedia http://en.wikipedia.org/wiki/Fluvastatin Link_out
ATC Codes
  • C10AA04
AHFS Codes
  • 24:06.08
PDB Entries Not Available
FDA label show (84.5 KB)
MSDS Not Available
Interactions
Drug Interactions
Drug Interaction
Acenocoumarol Fluvastatin may increase the anticoagulant effect of acenocoumarol. Monitor for changes in the therapeutic and adverse effects of acenocoumarol if fluvastatin is initiated, discontinued or dose changed.
Anisindione Fluvastatin may increase the anticoagulant effect of anisindione. Monitor for changes in the therapeutic and adverse effects of anisindione if fluvastatin if initiated, discontinued or dose changed.
Bezafibrate Increased risk of myopathy/rhabdomyolysis
Cholestyramine Increased/decreased effect according to spacing
Colchicine Increased risk of rhabdomyolysis with this combination
Colestipol Increased/decreased effect according to spacing
Cyclosporine Possible myopathy and rhabdomyolysis
Dicumarol Fluvastatin may increase the anticoagulant effect of dicumarol. Monitor for changes in the therapeutic and adverse effects of dicumarol if fluvastatin if initiated, discontinued or dose changed.
Eltrombopag Increases levels of Fluvastatin via metabolism decrease. OATP transporter protein inhibition.
Etravirine Fluvastatin, when administered concomitantly with etravirin, may experience an increase in serum concentration. It is recommended to monitor for signs of toxicity from fluvastatin, such as myopathy and hepatic enzyme elevations.
Fenofibrate Increased risk of myopathy/rhabdomyolysis
Fluconazole Fluconazole may increase the serum concentration of fluvastatin by decreasing its metabolism. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of fluvastatin if fluconazole is initiated, discontinued or dose changed.
Gemfibrozil Increased risk of myopathy/rhabdomyolysis
Rifabutin Rifabutin may decrease the effect of fluvastatin by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of fluvastatin if rifabutin is initiated, discontinued or dose changed.
Rifampin Rifampin may decrease the effect of fluvastatin by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of fluvastatin if rifampin is initiated, discontinued or dose changed.
Warfarin Fluvastatin may increase the anticoagulant effect of warfarin. Monitor for changes in the therapeutic and adverse effects of warfarin if fluvastatin is initiated, discontinued or dose changed.
Food Interactions
  • May be taken with or without food, but should be taken consistently.
Targets

1. 3-hydroxy-3-methylglutaryl-coenzyme A reductase

Pharmacological action: yes
Actions: inhibitor

This transmembrane glycoprotein is involved in the control of cholesterol biosynthesis. It is the rate-limiting enzyme of sterol biosynthesis

Organism class: human
UniProt ID: P04035 Link_out
Gene: HMGCR Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed
  2. Podar K, Tai YT, Hideshima T, Vallet S, Richardson PG, Anderson KC: Emerging therapies for multiple myeloma. Expert Opin Emerg Drugs. 2009 Mar;14(1):99-127. Pubmed
Enzymes

1. Cytochrome P450 3A4

Actions: substrate, inhibitor, inducer

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It performs a variety of oxidation reactions (e.g. caffeine 8-oxidation, omeprazole sulphoxidation, midazolam 1'-hydroxylation and midazolam 4- hydroxylation) of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. The enzyme also hydroxylates etoposide

UniProt ID: P08684 Link_out
Gene: CYP3A4
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Fischer V, Johanson L, Heitz F, Tullman R, Graham E, Baldeck JP, Robinson WT: The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor fluvastatin: effect on human cytochrome P-450 and implications for metabolic drug interactions. Drug Metab Dispos. 1999 Mar;27(3):410-6. Pubmed
  2. Toda T, Eliasson E, Ask B, Inotsume N, Rane A: Roles of different CYP enzymes in the formation of specific fluvastatin metabolites by human liver microsomes Basic Clin Pharmacol Toxicol. 2009 Nov;105(5):327-32. Pubmed
  3. Scripture CD, Pieper JA: Clinical pharmacokinetics of fluvastatin. Clin Pharmacokinet. 2001;40(4):263-81. Pubmed
  4. Zhou SF, Zhou ZW, Yang LP, Cai JP: Substrates, inducers, inhibitors and structure-activity relationships of human Cytochrome P450 2C9 and implications in drug development. Curr Med Chem. 2009;16(27):3480-675. Epub 2009 Sep 1. Pubmed
  5. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

2. Cytochrome P450 2C8

Actions: substrate, inhibitor

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. In the epoxidation of arachidonic acid it generates only 14,15- and 11,12-cis-epoxyeicosatrienoic acids. It is the principal enzyme responsible for the metabolism the anti- cancer drug paclitaxel (taxol)

UniProt ID: P10632 Link_out
Gene: CYP2C8
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Fischer V, Johanson L, Heitz F, Tullman R, Graham E, Baldeck JP, Robinson WT: The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor fluvastatin: effect on human cytochrome P-450 and implications for metabolic drug interactions. Drug Metab Dispos. 1999 Mar;27(3):410-6. Pubmed
  2. Toda T, Eliasson E, Ask B, Inotsume N, Rane A: Roles of different CYP enzymes in the formation of specific fluvastatin metabolites by human liver microsomes. Basic Clin Pharmacol Toxicol. 2009 Nov;105(5):327-32. Pubmed
  3. Scripture CD, Pieper JA: Clinical pharmacokinetics of fluvastatin. Clin Pharmacokinet. 2001;40(4):263-81. Pubmed
  4. Zhou SF, Zhou ZW, Yang LP, Cai JP: Substrates, inducers, inhibitors and structure-activity relationships of human Cytochrome P450 2C9 and implications in drug development. Curr Med Chem. 2009;16(27):3480-675. Epub 2009 Sep 1. Pubmed
  5. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

3. Cytochrome P450 2C9

Actions: substrate, inhibitor, inducer

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. This enzyme contributes to the wide pharmacokinetics variability of the metabolism of drugs such as S- warfarin, diclofenac, phenytoin, tolbutamide and losartan

UniProt ID: P11712 Link_out
Gene: CYP2C9
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Fischer V, Johanson L, Heitz F, Tullman R, Graham E, Baldeck JP, Robinson WT: The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor fluvastatin: effect on human cytochrome P-450 and implications for metabolic drug interactions. Drug Metab Dispos. 1999 Mar;27(3):410-6. Pubmed
  2. Toda T, Eliasson E, Ask B, Inotsume N, Rane A: Roles of different CYP enzymes in the formation of specific fluvastatin metabolites by human liver microsomes. Basic Clin Pharmacol Toxicol. 2009 Nov;105(5):327-32. Pubmed
  3. Scripture CD, Pieper JA: Clinical pharmacokinetics of fluvastatin. Clin Pharmacokinet. 2001;40(4):263-81. Pubmed
  4. Flockhart DA. Drug Interactions: Cytochrome P450 Drug Interaction Table. Indiana University School of Medicine (2007). Accessed May 28, 2010.
  5. Zhou SF, Zhou ZW, Yang LP, Cai JP: Substrates, inducers, inhibitors and structure-activity relationships of human Cytochrome P450 2C9 and implications in drug development. Curr Med Chem. 2009;16(27):3480-675. Epub 2009 Sep 1. Pubmed
  6. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

4. Cytochrome P450 2D6

Actions: substrate, inhibitor

Responsible for the metabolism of many drugs and environmental chemicals that it oxidizes. It is involved in the metabolism of drugs such as antiarrhythmics, adrenoceptor antagonists, and tricyclic antidepressants

UniProt ID: P10635 Link_out
Gene: CYP2D6 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Cohen LH, van Leeuwen RE, van Thiel GC, van Pelt JF, Yap SH: Equally potent inhibitors of cholesterol synthesis in human hepatocytes have distinguishable effects on different cytochrome P450 enzymes. Biopharm Drug Dispos. 2000 Dec;21(9):353-64. Pubmed
  2. Scripture CD, Pieper JA: Clinical pharmacokinetics of fluvastatin. Clin Pharmacokinet. 2001;40(4):263-81. Pubmed
  3. Zhou SF, Zhou ZW, Yang LP, Cai JP: Substrates, inducers, inhibitors and structure-activity relationships of human Cytochrome P450 2C9 and implications in drug development. Curr Med Chem. 2009;16(27):3480-675. Epub 2009 Sep 1. Pubmed
  4. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

5. Cytochrome P450 2C19

Actions: inhibitor

Responsible for the metabolism of a number of therapeutic agents such as the anticonvulsant drug S-mephenytoin, omeprazole, proguanil, certain barbiturates, diazepam, propranolol, citalopram and imipramine

UniProt ID: P33261 Link_out
Gene: CYP2C19 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Cohen LH, van Leeuwen RE, van Thiel GC, van Pelt JF, Yap SH: Equally potent inhibitors of cholesterol synthesis in human hepatocytes have distinguishable effects on different cytochrome P450 enzymes. Biopharm Drug Dispos. 2000 Dec;21(9):353-64. Pubmed

6. Cytochrome P450 1A1

Actions: substrate

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics

UniProt ID: P04798 Link_out
Gene: CYP1A1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Zhou SF, Zhou ZW, Yang LP, Cai JP: Substrates, inducers, inhibitors and structure-activity relationships of human Cytochrome P450 2C9 and implications in drug development. Curr Med Chem. 2009;16(27):3480-675. Epub 2009 Sep 1. Pubmed
  2. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

7. Cytochrome P450 2B6

Actions: inducer

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics

UniProt ID: P20813 Link_out
Gene: CYP2B6 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Zhou SF, Zhou ZW, Yang LP, Cai JP: Substrates, inducers, inhibitors and structure-activity relationships of human Cytochrome P450 2C9 and implications in drug development. Curr Med Chem. 2009;16(27):3480-675. Epub 2009 Sep 1. Pubmed

8. Cytochrome P450 1A2

Actions: inhibitor

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. Most active in catalyzing 2-hydroxylation. Caffeine is metabolized primarily by cytochrome CYP1A2 in the liver through an initial N3-demethylation. Also acts in the metabolism of aflatoxin B1 and acetaminophen

UniProt ID: P05177 Link_out
Gene: CYP1A2
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed
Transporters

1. Solute carrier organic anion transporter family member 1B1

Mediates the Na(+)-independent transport of organic anions such as pravastatin, taurocholate, methotrexate, dehydroepiandrosterone sulfate, 17-beta-glucuronosyl estradiol, estrone sulfate, prostaglandin E2, thromboxane B2, leukotriene C3, leukotriene E4, thyroxine and triiodothyronine. May play an important role in the clearance of bile acids and organic anions from the liver

UniProt ID: Q9Y6L6 Link_out
Gene: SLCO1B1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Kopplow K, Letschert K, Konig J, Walter B, Keppler D: Human hepatobiliary transport of organic anions analyzed by quadruple-transfected cells. Mol Pharmacol. 2005 Oct;68(4):1031-8. Epub 2005 Jul 26. Pubmed

2. Solute carrier organic anion transporter family member 1B3

Mediates the Na(+)-independent transport of organic anions such as 17-beta-glucuronosyl estradiol, taurocholate, triiodothyronine (T3), leukotriene C4, dehydroepiandrosterone sulfate (DHEAS), methotrexate and sulfobromophthalein (BSP)

UniProt ID: Q9NPD5 Link_out
Gene: SLCO1B3 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Kopplow K, Letschert K, Konig J, Walter B, Keppler D: Human hepatobiliary transport of organic anions analyzed by quadruple-transfected cells. Mol Pharmacol. 2005 Oct;68(4):1031-8. Epub 2005 Jul 26. Pubmed

3. Solute carrier organic anion transporter family member 2B1

Mediates the Na(+)-independent transport of organic anions such as taurocholate, the prostaglandins PGD2, PGE1, PGE2, leukotriene C4, thromboxane B2 and iloprost

UniProt ID: O94956 Link_out
Gene: SLCO2B1 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Kopplow K, Letschert K, Konig J, Walter B, Keppler D: Human hepatobiliary transport of organic anions analyzed by quadruple-transfected cells. Mol Pharmacol. 2005 Oct;68(4):1031-8. Epub 2005 Jul 26. Pubmed
Comments
Drug created on June 13, 2005 07:24 / Updated on March 03, 2013 16:38